Hence, METH-induced decreased Sigmar1 expression underlies the alteration in CREB/pCEBSer133/Fis1 signaling that adversely affects mitochondrial dynamics, morphometry, and respiration in cardiomyocytes, providing evidence for a pathogenic molecular mechanism in METH-induced cardiomyopathy. The gene discussed is CREB1; the disease is cardiomyopathy.